Exogenous application of methyl jasmonate induces defense response and develops tolerance against mungbean yellow mosaic India virus in Vigna mungo

2019 ◽  
Vol 46 (1) ◽  
pp. 69 ◽  
Author(s):  
Nibedita Chakraborty ◽  
Jolly Basak
Keyword(s):  
Methyl Jasmonate ◽  
Molecular Mechanisms ◽  
Stability Index ◽  
Protective Role ◽  
Membrane Stability ◽  
Vigna Mungo ◽  
Marker Genes ◽  
Exogenous Application ◽  
Ros Homeostasis

Vigna mungo (L.)Hepper is an economically important leguminous crop in south-east Asia. However, its production is severely affected by Mungbean yellow mosaic India virus (MYMIV). It is well established that methyl jasmonate (MeJA) is effective in inducing resistance against pathogens in several plants. To assess the role of MeJA in developing MYMIV tolerance in V. mungo, we analysed time-dependent biochemical and molecular responses of MYMIV susceptible V. mungo after exogenous application of different MeJA concentrations, followed by MYMIV infection. Our analysis revealed that exogenous application of different concentrations of MeJA resulted in decreased levels of malondialdehyde with higher membrane stability index values in MYMIV susceptible V. mungo, suggesting the protective role of MeJA through restoring the membrane stability. Moreover, the level of expression of different antioxidative enzymes revealed that exogenous MeJA is also very effective in ROS homeostasis maintenance. Enhanced expressions of the defence marker genes lipoxygenase and phenylalanine ammonia-lyase and the reduced expression of the MYMIV coat-protein encoding gene in all MeJA treated plants post MYMIV infection revealed that exogenous application of MeJA is effective for MYMIV tolerance in V. mungo. Our findings provide new insights into the physiological and molecular mechanisms of MYMIV tolerance in Vigna induced by MeJA.

Abstract MP13: TRPM7 Downregulation Contributes To Cardiovascular Injury And Hypertension Induced By Aldosterone And Salt

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Francisco J Rios ◽  
ZhiGuo Zou ◽  
Karla B Neves ◽  
Sarah S Nichol ◽  
Livia L Camargo ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Internal Diameter ◽  
Resistance Arteries ◽  
Cross Sectional ◽  
Vessel Structure ◽  
Cardiovascular Fibrosis ◽  
Fold Activation

TRPM7 has cation channel and kinase properties, is permeable to Mg 2+ , Ca 2+ , and Zn 2+ and is protective in the cardiovascular system. Hyperaldosteronism, which induces hypertension and cardiovascular fibrosis, is associated with Mg 2+ wasting. Here we questioned whether TRPM7 plays a role in aldosterone- induced hypertension and fibrosis and whether it influences cation regulation. Wild-type (WT) and TRPM7-deficient (M7+/Δ) mice were treated with aldosterone (600μg/Kg/day) and/or 1% NaCl (drinking water) (aldo, salt or aldo-salt) for 4 weeks. Blood pressure (BP) was evaluated by tail-cuff. Vessel structure was assessed by pressure myography. Molecular mechanisms were investigated in cardiac fibroblasts (CF) from WT and M7+/Δ mice. Protein expression was assessed by western-blot and histology. M7+/Δ mice exhibited reduced TRPM7 expression (30%) and phosphorylation (62%), levels that were recapitulated in WT aldo-salt mice. M7+/Δ exhibited increased BP by aldo, salt and aldo-salt (135-140mmHg) vs M7+/Δ-veh (117mmHg) (p<0.05), whereas in WT, BP was increased only by aldo-salt (134mmHg). Mesenteric resistance arteries from WT aldo-salt exhibited increased wall/lumen ratio (80%) and reduced internal diameter (15%) whereas vessels from M7+/Δ exhibited thinner walls by reducing cross-sectional area (35%) and increased internal diameter (23%) after aldo-salt. Aldo-salt induced greater collagen deposition in hearts (68%), kidneys (126%) and aortas (45%) from M7+/Δ vs WT. Hearts from M7+/Δ veh exhibited increased TGFβ, IL-11 and IL-6 (1.9-fold), p-Smad3 and p-Stat1 (1.5-fold) whereas in WT these effects were only found after aldo-salt. Cardiac expression of protein phosphatase magnesium-dependent 1A (PPM1A), a Mg 2+ -dependent phosphatase, was reduced (3-fold) only in M7+/Δ mice. M7+/Δ CF showed reduced proliferation (30%) and PPM1A (4-fold) and increased expression of TGFβ, IL-11 and IL-6 (2-3-fold), activation of Stat1 (2-fold), Smad3 (9-fold) and ERK1/2 (8-fold) compared with WT. Mg 2+ supplementation normalized cell proliferation and reduced protein phosphorylation in M7+/Δ CF (p<0.05). Our findings indicate a protective role of TRPM7 in aldosterone-salt induced cardiovascular injury through Mg 2+ -dependent mechanisms.

scholarly journals Protective role of α-actinin-3 in the response to an acute eccentric exercise bout

2010 ◽  
Vol 109 (2) ◽  
pp. 564-573 ◽  
Author(s):  
Barbara Vincent ◽  
An Windelinckx ◽  
Henri Nielens ◽  
Monique Ramaekers ◽  
Marc Van Leemputte ◽  
...  
Keyword(s):  
Muscle Damage ◽  
Eccentric Exercise ◽  
Stop Codon ◽  
Premature Stop Codon ◽  
Exercise Bout ◽  
Cell Number ◽  
Protective Role ◽  
Structural Function ◽  
Marker Genes

The ACTN3 gene encodes for the α-actinin-3 protein, which has an important structural function in the Z line of the sarcomere in fast muscle fibers. A premature stop codon (R577X) polymorphism in the ACTN3 gene causes a complete loss of the protein in XX homozygotes. This study investigates a possible role for the α-actinin-3 protein in protecting the fast fiber from eccentric damage and studies repair mechanisms after a single eccentric exercise bout. Nineteen healthy young men (10 XX, 9 RR) performed 4 series of 20 maximal eccentric knee extensions with both legs. Blood (creatine kinase; CK) and muscle biopsy samples were taken to study differential expression of several anabolic (MyoD1, myogenin, MRF4, Myf5, IGF-1), catabolic (myostatin, MAFbx, and MURF-1), and contraction-induced muscle damage marker genes [cysteine- and glycine-rich protein 3 (CSRP3), CARP, HSP70, and IL-6] as well as a calcineurin signaling pathway marker (RCAN1). Baseline mRNA content of CSRP3 and MyoD1 was 49 ± 12 and 67 ± 25% higher in the XX compared with the RR group ( P = 0.01–0.045). However, satellite cell number was not different between XX and RR individuals. After eccentric exercise, XX individuals tended to have higher serum CK activity ( P = 0.10) and had higher pain scores than RR individuals. However, CSRP3 ( P = 0.058) and MyoD1 ( P = 0.08) mRNA expression tended to be higher after training in RR individuals compared with XX α-actinin-3-deficient subjects. This study suggests a protective role of α-actinin-3 protein in muscle damage after eccentric training and an improved stress-sensor signaling, although effects are small.

scholarly journals Protective Role of Leaf Variegation in Pittosporum tobira under Low Temperature: Insights into the Physio-Biochemical and Molecular Mechanisms

2019 ◽  
Vol 20 (19) ◽  
pp. 4857
Author(s):  
Zhilu Zhang ◽  
Zhonghua Liu ◽  
Haina Song ◽  
Minghui Chen ◽  
Shiping Cheng
Keyword(s):  
Low Temperature ◽  
Molecular Mechanisms ◽  
Protective Role ◽  
Ros Scavenging ◽  
High Accumulation ◽  
Cold Response ◽  
Protective Function ◽  
Leaf Variegation ◽  
Pittosporum Tobira

Leaf variegation has been demonstrated to have adaptive functions such as cold tolerance. Pittosporum tobira is an ornamental plant with natural leaf variegated cultivars grown in temperate regions. Herein, we investigated the role of leaf variegation in low temperature responses by comparing variegated “Variegatum” and non-variegated “Green Pittosporum” cultivars. We found that leaf variegation is associated with impaired chloroplast development in the yellow sector, reduced chlorophyll content, strong accumulation of carotenoids and high levels of ROS. However, the photosynthetic efficiency was not obviously impaired in the variegated leaves. Also, leaf variegation plays low temperature protective function since “Variegatum” displayed strong and efficient ROS-scavenging enzymatic systems to buffer cold (10 °C)-induced damages. Transcriptome analysis under cold conditions revealed 309 differentially expressed genes between both cultivars. Distinctly, the strong cold response observed in “Variegatum” was essentially attributed to the up-regulation of HSP70/90 genes involved in cellular homeostasis; up-regulation of POD genes responsible for cell detoxification and up-regulation of FAD2 genes and subsequent down-regulation of GDSL genes leading to high accumulation of polyunsaturated fatty acids for cell membrane fluidity. Overall, our results indicated that leaf variegation is associated with changes in physiological, biochemical and molecular components playing low temperature protective function in P. tobira.

The Protective Role of Garlic on Allergen-Induced Airway Inflammation in Mice

2019 ◽  
Vol 47 (05) ◽  
pp. 1099-1112 ◽  
Author(s):  
Chia-Chen Hsieh ◽  
Wen-Huang Peng ◽  
Hsien-Hao Tseng ◽  
Shan-Yuan Liang ◽  
Li-Jen Chen ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Molecular Mechanisms ◽  
Chronic Respiratory Disease ◽  
Protective Role ◽  
Eosinophil Infiltration ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cytokines And Chemokines ◽  
Cell Counts ◽  
Bronchoalveolar Fluid

Asthma is the most prevalent chronic respiratory disease worldwide. Garlic extracts have long been used as a food source and in traditional medicine. Crude extracts of garlic are used as an anti-inflammatory agent and have been reported to exhibit antiasthmatic properties. However, molecular mechanisms of garlic extracts in the context of antiasthmatic airway inflammation are still unclear. In this study, the antiasthmatic effect of garlic extracts on Th1, Th2, and Th3 cytokine profiles and immunoregulatory mechanism were explored using an animal model of allergic asthma. Garlic extracts significantly reduced total inflammatory cell counts and eosinophil infiltration and decreased the production of Dermatophagoides pteronyssinus IgE in serum and Th1/Th2/Th3 cytokine in bronchoalveolar fluid. Enzyme-linked immunosorbent assay analysis demonstrated that garlic extracts downregulated the levels of cytokines and chemokines, namely Th2-related IL-4, IL-5, and IL-13; but they simultaneously upregulated Th1-related IFN-[Formula: see text], IL-12, and Th3-related IL-10 and TGF-[Formula: see text] expression in BALF. The mechanism may be ascribed to the modulation of Th1-, Th2-, and Th3-related cytokine imbalance.

Molecular mechanisms underlying protective role of quercetin in attenuating Alzheimer's disease

Life Sciences ◽  
2019 ◽  
Vol 224 ◽  
pp. 109-119 ◽  
Author(s):  
Elizabeta Zaplatic ◽  
Muhammed Bule ◽  
Syed Zahid Ali Shah ◽  
Md. Sahab Uddin ◽  
Kamal Niaz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Mechanisms ◽  
Protective Role

scholarly journals Protective Role of Malvidin-3-Glucoside on Peroxynitrite-Induced Damage in Endothelial Cells by Counteracting Reactive Species Formation and Apoptotic Mitochondrial Pathway

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Joana Paixão ◽  
Teresa C. P. Dinis ◽  
Leonor M. Almeida
Keyword(s):  
Endothelial Cells ◽  
Molecular Mechanisms ◽  
Mitochondrial Pathway ◽  
Protective Role ◽  
Reactive Species ◽  
Vascular Protection ◽  
Bax Protein ◽  
Species Formation ◽  
Mitochondrial Membrane Depolarization

The health-promoted benefits of anthocyanins, including vascular protective effects and antiatherogenic properties, have now been recognized, but the involved molecular mechanisms have not been well elucidated. Following our previous work on cytoprotective mechanisms of some anthocyanins against apoptosis triggered by peroxynitrite in endothelial cells, here we investigated the protective role of malvidin-3-glucoside, a major dietary anthocyanin, on such deleterious process, by exploring the interference on cellular reactive species formation and on apoptotic mitochondrial pathway. Preincubation of cells with 25 μM malvidin-3-glucoside protected efficiently endothelial cells from peroxynitrite-promoted apoptotic death, an effect which may be partially mediated by its ability to decrease the formation of reactive species after cell aggression, as assessed by the dichlorodihydrofluorescein diacetate assay and by carbonyl groups formation. Moreover, malvidin-3-glucoside inhibited mitochondrial apoptotic signaling pathways induced by peroxynitrite, by counteracting mitochondrial membrane depolarization, the activation of caspase-3 and -9, and the increase in the expression of the proapoptotic Bax protein. Altogether, our data expands our knowledge about the molecular mechanisms underlying the vascular protection afforded by malvidin-3-glucoside, and anthocyanins in general, in the context of prevention of endothelial dysfunction and atherosclerosis.

scholarly journals Sesamin Protects Against Cardiac Remodeling Via Sirt3/ROS Pathway

2017 ◽  
Vol 44 (6) ◽  
pp. 2212-2227 ◽  
Author(s):  
Di Fan ◽  
Zheng Yang ◽  
Fang-yuan Liu ◽  
Ya-Ge Jin ◽  
Ning Zhang ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Remodeling ◽  
Molecular Mechanisms ◽  
Nuclear Factor Κb ◽  
Protective Role ◽  
Control Group ◽  
Traditional Health ◽  
Smad2 Phosphorylation ◽  
Echocardiographic Parameters

Background/Aims: Cardiac remodeling is associated with oxidative stress. Sesamin, a well-known antioxidant from sesamin seeds, have been used extensively as traditional health foods. However, there is little known about the effect of sesamin on cardiac remodeling. Therefore, the present study aimed to determine whether sesamin could protect against cardiac remodeling and to clarify potential molecular mechanisms. Methods: The mice were subjected to either transverse aortic constriction (TAC) or sham surgery (control group). Beginning one week after surgery, the mice were oral gavage treated with sesamin (100mg·kg-1·day-1) or vehicle for 3 weeks. Cardiac hypertrophy was assessed by echocardiographic parameters, histological analyses and hypertrophic markers. Results: Sesamin alleviated cardiac hypertrophy, inhibited fibrosis and attenuated the inflammatory response. The increased production of reactive oxygen species, the activation of ERK1/2-dependent nuclear factor-κB and the increased level of Smad2 phosphorylation were observed in cardiac remolding model that were treated with sesamin. Furthermore, TAC induced alteration of Sirt3 and SOD2 was normalized by sesamin treatment. Finally, a selective Sirt3 inhibitor 3-TYP blocks all the protective role of sesamin, suggesting that a Sirt3-dependent effect of sesamin on cardiac remodeling. Conclusion: Sesamin improves cardiac function and prevents the development of cardiac hypertrophy via Sirt3/ROS pathway. Our results suggest the protective effect of sesamin on cardiac remolding.

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